Summary

C irculating platelet-leukocyte aggregates (PLA) were firstreported in the early 1960s (1) and long considered asbeing mere markers for vascular disease in which plateletactivation occurs (2–6). In this respect, an increase of PLA in thecirculation can be found under clinical conditions such as diabetes,hypertension (7), congestive heart failure (8), stroke (9) oracute coronary syndromes (10–12).Platelets are known to bind leukocytes via their P-selectin,which, upon cell activation, is translocated from the a -granulesto the cell surface (13–15). The main ligand for P-selectin isP-selectin Glycoprotein Ligand-1 (PSGL-1), a disulfide-linkedhomodimer constitutively expressed on most leukocytes(16–18). Also, integrin-mediated interactions via platelet glycoprotein(GP) IIb/IIIa – fibrinogen as bridging molecule as well asß z-integrin CD11b/CD18 (mac-1)or intercellular adhesion molecule-2 on leukocytes (19, 20), or via thrombospondin – plateletCD36 (GPIV) and leukocyte CD36 (21) are possible. Furthermore,immune complex interactions between platelet Fc?RII (CD32) and neutrophil Fc? RIIIb (22), as well as plateletGPIba and junctional adhesive molecule-C binding to leukocyte . . . .